ArticleScience signaling2024
The activation of the adaptor protein STING depends on its interactions with the phospholipid PI4P.
Article in Science signaling, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 33 citations in OpenAlex.
- Discovery of a novel STING-binding peptide associated with reduced cGAMP-induced inflammatory gene expression.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Mechanistic reprogramming of the mtDNA-cGAS-STING axis in cellular senescence: from mitochondrial homeostatic disruption to inflammatory and immune outcomes.Biogerontology · 2026Review
- Rejuvenating endogenous antitumor immunity via a chimeric receptor-engineered oncolytic virus targeting tumor-associated macrophages.Science advances · 2026Article
- Reciprocal control of viral infection and phosphoinositide dynamics.FEBS letters · 2026Review
- Spatial organization of phosphoinositide signaling.FEBS letters · 2026Review
- Chronic bisphenol A exposure activates the cGAS-STING-NLRP3 axis driving persistent hippocampal neuroinflammation and cognitive impairment.Molecular and cellular biochemistry · 2026Article
- The mutational landscape of STING-induced immunity.Nature · 2026Article
- Spatial control of NLRP3 inflammasome assembly by membrane lipid composition.Communications biology · 2026Review
- A lipid "glue" for STING oligomers.Cell research · 2026Article
- Dual Covalent Targeting of STING Cysteines 292/309 Disrupts Functional Oligomerization and Enables Potent Antagonist Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Apolipoproteins L involvement in immunity.Journal of human immunity · 2026Review
- PtdIns(3,5)PNature · 2026Article
- Article
- Distinct immune microenvironments in ovarian cancer subtypes indicate potential for immunotherapies.Journal of translational medicine · 2026Article
- PtdIns(3,5)PbioRxiv : the preprint server for biology · 2025Article
- Regulation of STING activation by phosphoinositide and cholesterol.bioRxiv : the preprint server for biology · 2025Article
- PRRs-Dependent and Independent Mechanisms of STING Signaling in Inflammatory and Autoimmune Diseases.Biomedicines · 2025Review
- Beyond interferons: Non-canonical roles of MITA/STING.Cell insight · 2025Review
- The scaffolding and activation of NLRP3 on acidic vesicles depends on their biophysical properties and is independent of intermediate filaments.Molecular biology of the cell · 2025Article
- Phosphatidylinositol 4-phosphate; A minor lipid with multiple personalities.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2025Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Activation of the endoplasmic reticulum (ER)-resident adaptor protein STING, a component of a cytosolic DNA-sensing pathway, induces the transcription of genes encoding type I interferons (IFNs) and other proinflammatory factors. Because STING is activated at the Golgi apparatus, control of the localization and activation of STING is important in stimulating antiviral and antitumor immune responses. Through a genome-wide CRISPR interference screen, we found that STING activation required the Golgi-resident protein ACBD3, which promotes the generation of phosphatidylinositol 4-phosphate (PI4P) at the trans-Golgi network, as well as other PI4P-associated proteins. Appropriate localization and activation of STING at the Golgi apparatus required ACBD3 and the PI4P-generating kinase PI4KB. In contrast, STING activation was enhanced when the lipid-shuttling protein OSBP, which removes PI4P from the Golgi apparatus, was inhibited by the US Food and Drug Administration-approved antifungal itraconazole. The increase in the abundance of STING-activating phospholipids at the trans-Golgi network resulted in the increased production of IFN-β and other cytokines in THP-1 cells. Furthermore, a mutant STING that could not bind to PI4P failed to traffic from the ER to the Golgi apparatus in response to a STING agonist, whereas forced relocalization of STING to PI4P-enriched areas elicited STING activation in the absence of stimulation with a STING agonist. Thus, PI4P is critical for STING activation, and manipulating PI4P abundance may therapeutically modulate STING-dependent immune responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.